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Comment on “Elevated House Dust and Serum Concentrations of PBDEs in California: Unintended Consequences of Furniture Flammability Standards?” Zota et al. (1) reported concentrations of polybrominated diphenyl ether (PBDE) congeners (BDE-47, -99, and -100) in house dust, and indicated California residents may have 2-fold higher PBDE blood levels than the national average. We provide context to the total concentration of the three bromodiphenyl ethers (BDEs) in dust from an exposure, toxicology, and risk assessment standpoint. Dust concentrations alone are inappropriate for deriving conclusions on exposure and risks. The United States (US) Environmental Protection Agency (EPA) sponsored a study of chemicals in dust collected from seven carpet layers, i.e., surface- and vacuum-dislodgeable, deeply embedded dust, carpet-fiber, -binder, and -padding, and on the subfloor beneath the carpet pad (2). The predominant reservoir was in layers not relevant to exposure, e.g., carpet fibers and binder. Relatively little, if any, residues were found on the surface. Residues bound to carpet fibers required organic extraction to liberate them, and deeply embedded dust was only acquired after 128 passes with a specially designed vacuum. Thus, determining the layer from which chemicals are measured is important; only surface- and vacuumdislodgeable residues are relevant for estimating exposure. Nonetheless, we assumed Zota et al.’s (1) results consisted of surface- and vacuum-dislodgeable residues only, and estimated exposures by (1) dividing BDE content by the number of days required to inhale the volume of air vacuumed, or (2) calculating the median and maximum BDE intake based on a child’s consumption of 60 mg of dust/day. Method 1 produced exposures below reference values (Table S1-S2). The American Society for Testing and Materials International guidance for measuring vacuum-dislodgeable residues from carpets specifies a vacuum with an airflow of 26.5 cubic feet/minute (CFM) (3). A model similar to Zota et al.’s (1) has an airflow of 135 CFM, and would produce samples with deeply embedded dust. At a vacuumed air volume of 172 m3, the median dust intake is 1,516-2,382 ng/day. Daily intake at the EPA’s Integrated Risk Information System’s (IRIS) chronic oral reference dose (RfD), 2,280-6,360 ng/day, exceeds the estimated exposures. Zota et al.’s (1) maximum values, which are not representative of an individual’s lifetime exposure, were compared to the US Agency for Toxic Substances and Disease Registry’s (ATSDR) intermediate oral minimal risk level (MRL) (Table S1-S1). The estimated intakes are below levels that are without appreciable risks. Method 2 indicates de minimis risks; i.e., ∼500 ng/day compared to that at EPA’s chronic RfDs or ATSDR’s lessthan-lifetime reference value (Table S1-S2). Regarding possible perturbation of thyroid hormones, IRIS derived their RfDs for tetra-, penta-, hexa-, and deca-BDE from developmental neurotoxicity studies (4-7) that treated siblings as independent variables, a practice that increases the false-positive rate (8-13). ATSDR’s MRL for penta-BDE was derived from a rat 90-day dietary study with a 300-fold uncertainty factor applied to the lowest effect dose (2 mg/ kg-day; hepatic hypertrophy, mild degeneration, and slight necrosis). Reductions in serum T4 levels were only noted at g10 mg/kg-day. ATSDR interpreted this effect as a likely indirect consequence of hepatic enzyme induction. Thus, 10.1021/es803313q CCC: $40.75
Published on Web 02/25/2009
2009 American Chemical Society
changes in thyroid hormone levels are adequately protected against by reference values derived from studies using an experimental design prone to false positives (i.e., IRIS’ RfDs) or based on a precursor effect (i.e., ATSDR’s MRL). We also note Zota et al.’s (1) mention of the study linking hyperthyroidism and PBDE exposure in California cats (14). A major discrepancy with that study is that while a few PBDE congeners have been shown to lower T4 blood levels in rats (construed as hypothyroidism), none have been shown to cause hyperthyroidism. Zota et al.’s (1) reported concentrations of BDEs in house dust must be interpreted cautiously. The dust collection methodology was inappropriate for assessing exposure. Nonetheless, the reported BDE dust concentrations would produce exposures below established reference values. Though the authors reported blood levels of California residents were above the national average, it is important to consider that detection does not equate to risk.
Disclosure of Conflicts of Interest M.B. received an honorarium from Albemarle Corporation for work on a previous manuscript. No form of remuneration was provided for his work herein. J.B. and J.M.A. are employed by Chemtura Corporation, a specialty chemical manufacturer whose product lines include brominated flame retardants. R.D.H., C.G.H., and D.J.P. have no conflicts to declare. M.H. and T.S. are employed by Albemarle Corporation, a specialty chemical manufacturer whose product lines include brominated flame retardants. The views and opinions expressed in this article are those of the authors and not necessarily those of Institute of Public Health and Environmental Protection, Chemtura Corporation, University of South Florida, US Army, Environmental Protection Commission of Hillsborough Countv, or the Albemarle Corporation.
Supporting Information Available Table S1-S2. This material is available free of charge via the Internet at http://pubs.acs.org.
Literature Cited (1) Zota, A. R.; Rudel, R. A.; Morello-Frosch, R. A.; Brody, J. G. Elevated house dust and serum concentrations of PBDEs in California: Unintended consequences of furniture flammability standards? Environ. Sci. Technol. 2008, 42 (21), 8158– 8164. (2) EPA. Analysis of Aged In-Home Carpeting to Determine the Distribution of Pesticide Residues between Dust, Carpet, and Pad Compartments; EPA/600/R-00/030; National Exposure Research Laboratory: Research Triangle Park, NC, 2000. (3) ASTM International. Standard Practice for Collection of Floor Dust for Chemical Analysis; Designation D 5438-05; ASTM International: West Conshohocken, PA, 2005. (4) Eriksson, P.; Jakobsson, E.; Fredriksson, A. Brominated flame retardants: a novel class of developmental neurotoxicants in our environment? Environ. Health Perspect. 2001, 109(9), 903– 908. (5) Viberg, H.; Frederiksson, A.; Eriksson, P. Investigations of strain and/or gender differences in developmental neurotoxic effects of polybrominated diphenyl ethers in mice. Toxicol. Sci. 2004, 81 (2), 344–353. (6) Viberg, H.; Fredriksson, A.; Eriksson, P. Neonatal exposure to polybrominated diphenyl ether (PBDE 153) disrupts spontaneous behaviour, impairs learning and memory, and decreases hippocampal cholinergic receptors in adult mice. Toxicol. Appl. Pharmacol. 2003, 192 (2), 95–106. ¨ rn, U.; Eriksson, (7) Viberg, H.; Fredriksson, A.; Jakobsson, E.; O P. Neurobehavioral derangements in adult mice receiving decabrominated diphenyl ether (PBDE 209) during a defined VOL. 43, NO. 7, 2009 / ENVIRONMENTAL SCIENCE & TECHNOLOGY
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John Biesemeier Environmental Health, Safety & Security, and Regulatory Affairs & Toxicology, Chemtura Corporation, West Lafayette, Indiana
John M. Ariano Polymer Additives, Chemtura Corporation, West Lafayette, Indiana
Raymond D. Harbison Center for Environmental and Occupational Risk Analysis and Management, College of Public Health, University of South Florida, Tampa, Florida
Carl G. Hover Safety, Environment and Integrated Planning Office, US Army, Fort Detrick, Maryland
Debra J. Price Air Management Division, Environmental Protection Commission of Hillsborough County, Tampa, Florida
Marcia Hardy and Todd Stedeford Marek Banasik Institute of Public Health and Environmental Protection, Warsaw, Poland
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Health, Safety & Environment, Albemarle Corporation, Baton Rouge, Louisiana ES803313Q
